This title appears in the Scientific Report : 2010 

Human amygdale reactivity is diminished by the beta-noradrenergic antagonist propranolol
Hurlemann, R.
Walter, H. / Rehme, A.K. / Kukolja, J. / Santoro, S.C. / Schmidt, C. / Schnell, K. / Musshoff, F. / Keysers, C. / Maier, W. / Kendrick, K.M. / Onur, O.A.
Kognitive Neurowissenschaften; INM-3
Psychological medicine, 40 (2010) S. 1839 - 1848
Cambridge Cambridge Univ. Press 2010
1839 - 1848
20102667
10.1017/S0033291709992376
Journal Article
(Dys-)function and Plasticity
Funktion und Dysfunktion des Nervensystems
Psychological Medicine 40
J
Please use the identifier: http://dx.doi.org/10.1017/S0033291709992376 in citations.
Animal models of anxiety disorders emphasize the crucial role of locus ceruleus-noradrenergic (norepinephrine, NE) signaling, the basolateral amygdala (BLA) and their interactions in the expression of anxiety-like behavioral responses to stress. Despite clinical evidence for the efficacy of a β-noradrenergic receptor blockade with propranolol in the alleviation of anxiety symptoms and the secondary prevention of post traumatic stress disorder, preclinical evidence for a β-noradrenergic modulation of BLA activity in humans is missing.We combined functional magnetic resonance imaging in healthy volunteers with probabilistic mapping of intra-amygdalar responses to fearful, neutral and happy facial expressions to test the hypothesis that a β-noradrenergic receptor blockade with propranolol would inactivate the BLA.Consistent with our a priori hypothesis, propranolol diminished BLA responses to facial expressions, independent of their emotional valence. The absence of activity changes in probabilistically defined visual control regions underscores the specific action of propranolol in the BLA.Our findings provide the missing link between the anxiolytic potential of propranolol and the biological basis of β-noradrenergic activation in the human BLA as a key target for the pharmacological inhibition of anxiety neurocircuitry. Moreover, our findings add to emerging evidence that NE modulates both the reactivity (sensitivity) and the operating characteristics (specificity) of the BLA via β-noradrenergic receptors.